Genetic Polymorphism, Platelet Reactivity and Clinical Outcomes after Percutaneous Coronary Intervention in Ischemic Heart Disease Patients

The aim of this study was to assess platelet reactivity considering the CYP2C19*2/3 genetic and platelet functional tests in patients with stable coronary artery disease (SCAD) underwent percutaneous coronary intervention (PCI).
Methods: 55 (SCAD) patients (39 -75 y.o., mean 59±9.68 y.o.) were studied before and after PCI procedures. Beside conventional investigations, antiplatelet therapy efficacy was assessed by Thromboelastogrphy (TEG) and panel Рlаtеlеt Мaррing with arachidonic acid and ADP–induced platelet aggregation and light transmission aggregometry. Detecting a genetic polymorphism in CYP2C19*2 and CYP2C19*3 were held using allele- specific polymerase chain reaction at the end of follow-up period (mean 24 months).
Results: Our analysis revealed a normal genotype (GG) in 39 patients, heterozygous polymorphisms CYP2C19 (GA) G681A allele were detected in 14 patients, and 2 patients has homozygous polymorphisms CYP2C19 (AA) G681A allele. All 55 patients in study had normal CYP2C19*3 (Trp212Ter) genotype of CYP2C19 gene. The platelet activation was higher in patients with heterozygous and homozygous carriers comparing to normal genotype: the largest differences were in groups with different genotype (GG, GA, AA). We revealed a statistically significant influence of various genotypes of CYP2C19 * 2 (GG, GA, AA) on the average values of platelet aggregation (p = 0,02). Also a reliable relationship between MACE and the platelet aggregation according to the LTA (p = 0,002) was obtained. In our study there was no significant relationship between the different genotypes CYP2C19*2 and the average values ​​of PRU (p=0,057), however, their joint impact on MACE was statistically significant (p = 0,041).
Conclusions: The levels of platelet reactivity were higher in heterozygous and homozygous carriers of CYP2C19*2 genotype; the latest with high on-treatment platelet reactivity had a significantly increased risk of MACE during follow-up.